Division of Nanomedicine and Molecular Intervention, Department of Medicine, Michigan State University, East Lansing, MI, U.S.A.
Neuroscience Program, Michigan State University, East Lansing, MI, U.S.A.
In Vivo. 2020 Sep-Oct;34(5):2259-2268. doi: 10.21873/invivo.12036.
BACKGROUND/AIM: Transient receptor potential vanilloid type 1 (TRPV1) has anti-inflammatory properties. The present study aimed to investigate the role of TRPV1 in renal inflammatory responses and tissue injury following renal ischemia-reperfusion (I/R) in diet-induced obese mice.
TRPV1 knockout and wild type mice were fed a normal or western diet (WD) for 23 weeks and were then subjected to renal I/R injury.
TRPV1 knockout mice showed enhanced WD-induced renal macrophage infiltration and collagen deposition. Knocking out TRPV1 exacerbated renal I/R-induced increase of malondialdehyde, interleukin-6, monocyte chemoattractant protein-1, and NF-ĸB in obese mice. Similar results were observed in the expression of phosphorylated Smad1 and Smad2/3. Blockade of calcitonin gene-related peptide (CGRP) receptors with CGRP8-37 worsened the I/R-induced renal inflammation and injury.
Our data indicate that preserving TRPV1 expression and function may prevent renal I/R injury in obesity likely through alleviating inflammatory responses.
背景/目的：瞬时受体电位香草酸亚型 1（TRPV1）具有抗炎作用。本研究旨在探讨 TRPV1 在饮食诱导肥胖小鼠肾缺血再灌注（I/R）后肾炎症反应和组织损伤中的作用。
TRPV1 敲除和野生型小鼠分别喂食正常或西方饮食（WD）23 周，然后进行肾 I/R 损伤。
TRPV1 敲除小鼠表现出增强的 WD 诱导的肾巨噬细胞浸润和胶原沉积。在肥胖小鼠中，敲除 TRPV1 加剧了肾 I/R 诱导的丙二醛、白细胞介素-6、单核细胞趋化蛋白-1 和 NF-ĸB 的增加。磷酸化 Smad1 和 Smad2/3 的表达也观察到类似的结果。用 CGRP8-37 阻断降钙素基因相关肽（CGRP）受体加重了 I/R 引起的肾炎症和损伤。
我们的数据表明，保留 TRPV1 的表达和功能可能通过减轻炎症反应来预防肥胖引起的肾 I/R 损伤。
